The purpose of this research is to develop a better understanding of the physiological basis for neuroendocrine control of the onset of puberty and gonadotropin secretion in the monkey (Macaca fascicularis). Our studies of puberty have three specific objectives: (1) to isolate the neural structures important in the development of the onset of neuroendocrine puberty in primates; (2) to determine whether pulsatile administration of exogenous LHRH can initiate the development of the neuroendocrine substrate mediating both positive and negative feedback effects of estrogen; and (3) to develop a model of androgen-mediated sexual precocity with respect to both negative- and positive-feedback regulation by estrogens. To fulfill these objectives we will use the prepubescent female macaque as our experimental model and perform selective brain lesions and steroid manipulations to modify and control the onset of puberty. Our studies of gonadotropin regulation in the male primate are directed toward the attainment of two specific goals: (1) to explore the role of LHRH-signal processing (pulse frequency, rate-of-change, width, amplitude) by the pituitary gonadotrope as one mechanism of LHRH action on the differential regulation of the LH and FSH secretion, and to determine whether pulsatile administration of LHRH can selectively elevate plasma FSH over LH concentration in the adult male; and (2) to define the role of the pituitary gland as one important site of negative feedback effects of testicular steroids. We will use the adult male macaque as our experimental model. These animals will be lesioned in the arouate nucleus, and thus will be LHRH deficient. The lesson isolates the pituitary gland from hypothalamic LHRH input and would enable a clearer resolution of the question of LHRH-pituitary interaction and steroid-pituitary feedback control. A demonstration that a particular LHRH pulse frequency (or other signal variable) can cause a selective increase in FSH over LH would offer one explanation of how a single releasing factor can differentially control both LH and FSH secretion. A resolution of these problems is fundamental to our greater understanding of the basic physiology of the neuroendocrine control of reproduction.